The purpose of this project is to investigate the concentrations of histamine in whole blood and ascorbic acid in the blood plasma of normal unstressed people on a normal diet without dietary supplements, in people with unstable angina and in people with acute myocardial infarction, to test the hypothesis that histamine plays a key role in the development of atherosclerosis and coronary heart disease. Studies in the second year will include attempts at preventing heart attacks by controlling blood histamine levels. Until recently, it was thought that vitamin C depletion was of little physiologic consequence until there was a complete absence of the vitamin, presenting as classical scurvy. However, it is now known that blood histamine levels begin to rise when plasma ascorbate levels are barely suboptimal both in guinea pigs and in man. Blood histamine levels begin to rise when the plasma ascorbic levels fall below normal (1mg/100ml) and is doubled when plasma ascorbate falls below 0.7mg/ml. Blood histamine concentration is quadrupled when ascorbate levels fall below 0.2mg/100ml and rises even higher under the influence of sleep deprivation or other forms of physical or psychological stress. These observations are of particular importance, as both histaminemia and vitamin C-deficiency cause diastasis or separation of vascular endothelial cells of the aorta, and other blood vessels. Vitamin C-deficiency is commonly thought of causing hemorrhage rather than thrombosis. But the hemorrhage associated with vitamin C-deficiency is due to vascular damage and thrombosis is the mechanism for the arrest of this hemorrhage. Moreover, the coagulation mechanism in scurvy for the most part is intact.